Patients with Bartter's syndrome are resistant to the pressor effects of angiotensin II and of norepinephrine. The observations that resistance to these vasopressors is present in patients with other disorders characterized by hypokalemia and an overproduction of prostaglandins and that pressor responsiveness to these vasopressors may be restored to normal by treatment with a prostaglandin synthetase inhibitor suggest that vasodilator prostaglandins synthesized by vascular tissue may, in part, be responsible for the pressor resistance in Bartter's syndrome. The finding of an increased excretion of norepinephrine and epinephrine in the urine of patients with Bartter's syndrome suggests that the pressor resistance to norepinephrine may be associated with an increase in activity of the sympathetic nervous system.